13.4
1.
a.
Gamma-amino butyric acid: the primary inhibitory neurotransmitter of the central nervous
system, making postsynaptic neurons less likely to be activated
Found mostly in the brain e.g. widely distributed
b.
The particular role of GABA relevant to specific phobia is its inhibitory effect on postsynaptic
neurons. It balances the excitatory effect of glutamate that can be associated with anxiety
e.g. GABA is believed to control the fear or anxiety experienced when neurons are
overexcited. This role is supported by research evidence (e.g. clinical
trials) that the medications used to alleviate anxiety, such as Valium and Xanax, bind to the
same neuronal receptors as GABA. The effect of these benzodiazepine medications is to
enhance the natural effect of GABA, thereby helping GABA to reduce neural activity even
further.
c.
Gamma-amino butyric acid (GABA) dysfunction: failure to produce, release or receive
sufficient levels/the correct amount of GABA needed to regulate neuronal transmission in the
brain, particularly to counterbalance the excitatory activity of glutamate
d.
GABA plays a role in in anxiety because it acts like a calming agent or ‘brake’ to the
excitatory activity of neurotransmitters in the brain that contribute to anxiety.People with low
levels of GABA tend to be more vulnerable to anxiety and their fight–flight–freeze response
may be more easily activated, thus making them more susceptible to developing phobias
and/or maintaining symptoms compared to people with normal or higher levels of GABA
production.GABA agonists/benzodiazepines alleviate fear or anxiety symptoms, thereby
providing evidence of a contributory role of GABA dysfunction
2.
a.
A common reaction to a perceived threat/fearful stimulus is a physiological stress response
involving fight or flight or freeze, particularly flight. When this occurs, sympathetic nervous
system responses are activated e.g. increased heart and respiration rates, secretion of
stress hormones etc. to energise the body and support flight or fight if required.
b.
GABA dysfunction involves failure to produce, release or receive sufficient levels/the correct
amount of GABA needed to regulate neuronal transmission in the brain. If GABA production
is significantly lower than required, then the excitatory activity of glutamate and other
neurotransmitters that contribute to anxiety and excessive fight–flight sympathetic nervous
system reactions cannot be counterbalanced/calmed.
c.
memory bias and catastrophic thinking
3.
long-term potentiation can neurologically strengthen the association between a phobic
stimulus and a fear or anxiety response through its activity at synapses within a neural
pathway for the phobic reaction. The more that the connections are activated through each
encounter with a phobic stimulus, the more the connections are strengthened, increasing the
efficiency in transferring fear information along the pathway and decreasing the likelihood
that the fear response can be forgotten.
4.
GABA
dysfunction
failure to produce, release or
receive sufficient amount of
GABA to regulate neuronal
transmission in the brain,
particularly to counterbalance
the excitatory activity of
glutamate
cannot adequately counterbalance
the excitatory effect of glutamate
associated with anxiety e.g. GABA is
believed to control the fear or anxiety
experienced when neurons are
overexcited
stress
response
physiological reaction to a
perceived threat/fearful
stimulus involving fight or flight
or freeze, particularly
sympathetic nervous system
activity associated with flight
i.e. need for avoidance
activated even when the individual is
not actually facing any real threat or
danger; the bodily changes (e.g.
pounding heart, abnormal breathing)
may heighten the fear/anxiety and
maintain symptoms of the phobic
reaction; the bodily changes may
become a conditioned response to a
phobic stimulus
long-term
potentiation
the long-lasting strengthening
of synaptic connections
through activity at the synapse,
resulting in enhanced or more
effective synaptic transmission
the more that the connection is
activated through each encounter
with a phobic stimulus, the more the
connection is strengthened,
increasing the efficiency in
transferring fear information along
the relevant neural pathway and
decreasing the likelihood that the
fear response can be forgotten